The development of knock-out mice for Angiotensin II (Ang II) AT 2 receptors, which exhibited altered exploratory behavior, prompted us to investigate the cerebellum and brainstem. We evaluated the effect of stimulation/inhibition of Ang II receptors on hindbrain development, in offspring (postnatal days P0, P8) of pregnant rats treated during late pregnancy (Ang II, Losartan or PD123319, 1 mg/kg/day). Receptor localization by autoradiography showed in P0 and P8 hindbrains, that most structures expressed AT 2 subtype: cerebellar cortex, cerebellar nuclei, genu facial nucleus, inferior colicullus, inferior olive. In the cerebellar cortex, [ 125 I]Ang II AT 2 binding was predominant, while low AT 1 binding was observed in adjacent layers of the cerebellar cortex. Blockade of AT 2 receptors with PD123319 increased binding in cerebellar nuclei (p<0.05) and brainstem nuclei at P0, P8, in correlation with increased AT 2 receptor expression by RT-PCR. The enlarged external granular layer (EGL) in PD123319-treated P0 pups contrast with the significant decrease in Ang II binding (p<0.001) in the cerebellar cortex. Blockade of AT 2 receptors during late pregnancy seems to arrest cerebellar cortex development in P0 animals. On the contrary, increased AT 2 binding was observed in cerebellar cortex and DTg nucleus in PD123319-treated P8 animals (p<0.001). Ang II treatment leads to increased binding in the brainstem. In spite of the low doses of Ang II antagonists used, treatments were performed during a time-frame critical for hindbrain development, leading to remarkable effects. The present study makes a contribution to understand the role of Ang II receptors during hindbrain development.